Abstract

Abstract Introduction Lipoprotein A (LpA) is considered a cardiovascular disease (CVD) risk factor and its interest has grown in recent years. High LpA levels (above 50 mg/dL) are associated with an increase in the occurrence of CVD and degenerative aortic valve disease despite treatment with statins and low LDL levels. The prevalence of elevated LpA levels after heart transplantation (HT) and the implication on the development of cardiac allograft vasculopathy (CAV) is not well known. Objective To assess the prevalence of elevated LpA levels in patients with HT and the relationship between higher LpA levels and CAV at 1 year. Methods Retrospective, unicentric and observational study based on the historical cohort of HT patients. We selected those patients in whom a pre-transplant serum sample was available in the biobank for LpA analysis. CAV was diagnosed with coronary angiography. Results We studied 80 HT patients. Baseline characteristics are in table 1. Median LpA levels were 14.5 (5.0-35.3), and from the 80 HT patients, 16 (20,0%) had LpA≥50 mg/dl (figure 1A). Out of the 80 patients, 68 had a coronary angiography at 1 year follow up (3 died before 1 year and 9 patients did not have angiography at 1 year for diverse reasons). Twenty patients (29.4%) presented CAV in the first year. Patients with elevated LpA levels had more frequency of CAV at 1 year [11/16 (68.8%) vs 9/43 (17.3%); p<0,001]. LpA levels in patients with CAV was higher (62.5+-58.8 vs 23.9+29.8; p<0,001) (figure 1B). LDLc and Total cholesterol were significantly lower in patients with CAV at 1 year in this population. In univariate analysis, smoker donors were associated with CAV development (60.0% vs 33.3%; p 0.042). We did not find differences in other recipient or donor cardiovascular risk factors, rejection episodes or CMV infection in the first year. Conclusion Elevated LpA levels (≥50 mg/dl) are frequent in HT patients (20%) and in our cohort, were associated with CAV at 1-year post-HT. Further studies are needed to verify these results and study the relationship with the development of other cardiovascular events in HT patients.Table 1Figure 1

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